Atopic patients have an array of autonomic abnormalities including cholinergic hyperresponsivity and Beta-adrenergic hyporeactivity. Rabbits immunized in a manner leading to selective IgE production were found to concomitantly develop cholinergic hyperreactivity suggesting a link between the immunologic and neurophysiologic abnormalities. Subjects with Beta-adrenergic hyporeactivity (atopic and others) were found to have antibodies directed at their Beta-adrenergic receptors possibly providing a mechanism for the neurophysiologic disturbance. Peripheral blood PMN and lymphocytes were found to lack demonstrable alpha-adrenergic receptors, but PMN do have histamine H-1 receptors. During the course of these studies, a technique for the rapid isolation of platelet-free lymphocytes from blood was developed. Plasma histamine (normal) = 318 + or - 25 pg/ml and patients with systemic mastocytosis have marked elevations. Late phase allergic reactions were found to be dependent on early PMN infiltration, independent of complement and inhibited by combinations of H-1 and H-2 antihistamines.